A parallel occlusion of one of the branch arterioles induces vasodilation in the opposite unoccluded branch. Increases in flow and wall share rate in the unoccluded branch by the parallel occlusion has been thought to be one of the primary causes of vasodilation. This dilation induced by the parallel occlusion has been referred to as evidence that flow-induced dilation plays a significant role in diameter control on the microvascular network. However, there are some studies which argue that mechanisms other than the flow induced dilation is involved in the vasodilation observed in microcirculation during parallel occlusion. The purpose of this study is readdressing the role of flow induced dilation during parallel occlusion by focusing on delay times between increase in flow velocity and vasodilation during parallel occlusion. The differences of flow induced dilation and myogenic responses among different skeletal muscles are also analyzed.In 23 of the 40 occlusions, diameter of unoccluded arterioles dilated immediately after onset of parallel occlusion with increases in diameter (18.1 +/-4.51 % of control), WSR (65.7 +/-8.91 %), velocity (80.5 +/-8.47 % of control) and flow (153.4 +/-23.2 % of control). In the rest of the 17 occlusions, arterioles dilated with 8.8 +/-1.1 sec of delay time after the onset of occlusion. In these cases, the increases in diameter (22.1 +/-2.51 %), WSR (117.8 +/-22.8 %), velocity (119.1 +/-17.8 %) and flow (241.6 +/-26.8 %) from the control were significantly higher than the increase in the values observed without delay time. From these results, we concluded that the dilation with or without delay time from onset of the occlusion is functionally different. Thus, delay. time is a crucial index to identify the flow induced dilation. We also suggest that location of the arterioles affects the response of myogenic and flow induced vascular activities to changes in flow velocity and transmural pressure.